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Foxb1-expressing neurons occur in the dorsal premammillary nucleus (PMd) and further rostrally in the parvafox nucleus, a longitudinal cluster of neurons in the lateral hypothalamus of rodents. The descending projection of these Foxb1+neurons end in the dorsolateral part of the periaqueductal gray (dlPAG). The functional role of the Foxb1+neuronal subpopulation in the PMd and the parvafox nucleus remains elusive. In this study, the activity of the Foxb1+neurons and of their terminal endings in the dlPAG was selectively altered by employing chemo- and optogenetic tools. Our results show that in whole-body barometric plethysmography, hM3Dq-mediated, global Foxb1+neuron excitation activates respiration. Time-resolved optogenetic gain-of-function manipulation of the terminal endings of Foxb1+neurons in the rostral third of the dlPAG leads to abrupt immobility and bradycardia. Chemogenetic activation of Foxb1+cell bodies and ChR2-mediated excitation of their axonal endings in the dlPAG led to a phenotypical presentation congruent with a “freezing-like” situation during innate defensive behavior.Contact and competing interest information for all authorsContact: Marco R. Celio, marco.celio@unifr.ch. The authors have no relevant financial or non-financial interests to disclose.Data sharing plansDue to their storage in a university database, the datasets generated during the current study are not publicly available but are available from the corresponding author on reasonable request.Funding supportThis work was supported by the Swiss National Foundation grant 31003A_160325 to Marco R. Celio. |
